Cancer treatment, and melanoma treatment in particular, is being revolutionized by the development of effective immunotherapeutic approaches (Kaufman, H. L. et al. Nature reviews. Clinical oncology 10, 588-598 (2013); Mellman et al. Nature 480, 480-489 (2011).; herein incorporated by reference in their entireties). These strategies include blockade of immune-inhibitory receptors on activated T cells, for example using monoclonal antibodies (mAbs) against CTLA-4 and PD-1/PD-L1 (Wolchok, J. D. et al. The New England Journal of Medicine 369, 122-133 (2013); Topalian, S. L. et al. Journal of clinical oncology 32, 1020-1030 (2014); Topalian, S. L. et al. The New England journal of medicine 366, 2443-2454 (2012); Hodi, F. S. et al. The New England journal of medicine 363, 711-723 (2010); herein incorporated by reference in their entireties). However, only a subset of patients responds to these treatments, and data suggest that therapeutic benefit is preferentially achieved in patients who have a pre-existing T cell response against their tumor as evidenced by a baseline CD8+ T cell-infiltration within the tumor-microenvironment (Harlin, H. et al. Cancer research 69, 3077-3085 (2009); Ji, R. R. et al. Cancer immunology, immunotherapy: CII 61, 1019-1031 (2012); Gajewski et al. Cancer journal 16, 399-403 (2010); herein incorporated by reference in their entireties). What is needed in the field is an understanding of the molecular mechanisms that underlie the presence or absence of a spontaneous anti-tumor T cell response in subsets of cases, and therapeutic solutions for patients lacking a T cell infiltrate.